Kyushu University Academic Staff Educational and Research Activities Database
List of Presentations
Koichiro Matsumoto Last modified date:2019.06.26

Associate Professor / Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University / Research Institute for Deseases of the Chest / Faculty of Medical Sciences


Presentations
1. 松元 幸一郎, Interleukin-22 downregulates double-stranded RNA-induced expression of B7-H1/PD-L1 on airway epithelial cells, 2014.09, Background and Aim: Airway viral infection is a cause of exacerbations of COPD. B7-H1/PD-L1 is a coinhibitory molecule implicated in an escape mechanism of viruses from the host immune systems. Molecules suppressing expression of B7-H1/PD-L1 may be preventive for virus-induced exacerbation. Interleukin-22 (IL-22) is a member of the IL-10 family that is produced from a variety of immune cells and has protective properties on tissue-structural cells including epithelial cells. We investigated the effect of IL-22 on the expression of B7-H1/PD-L1.
Methods: Airway epithelial cell lines were treated with or without an analog of viral double-stranded RNA, polyinosinic-polycytidylic acid (poly I:C) in the presence or absence of human IL-22. The expression of B7-H1/PD-L1 was assessed by flow cytometry.
Results: The expression of B7-H1/PD-L1 was upregulated by poly I:C in a dose-dependent manner. The magnitude of B7-H1/PD-L1 expression remained constant from 24h to 48h after the stimulation of poly I:C. Without poly I:C, the expression of B7-H1/PD-L1 was not affected by treatment with IL-22. Poly I:C-induced upregultaion of B7-H1/PD-L1 was significantly attenuated by treatment with IL-22.
Conclusion: IL-22 downregluates double-stranded RNA-induced expression of B7-H1/PD-L1 on airway epithelial cells, suggesting a beneficial role of IL-22 in virus-associated pathogenesis of COPD. The examinations for in vivo effect of IL-22 is underway using a murine model of poly I:C-induced inflammation.
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